This paper on the genetics of human pair bonding came out last week. The idea that genes affect behaviour is not a new one, but the extent of their influence is argued over. Usually it is evangelicals, whose world view is dependant on the absurd notion of free will and its implications for “sin”, that make loud denial noises at the thought that our choice making may not be absolutely free. Another problem they have is that if our genes affect our behaviour and personality, then the mind becomes all the more physical and ideas of a supernatural consciousness become even less likely. From studies on flies, sexual orientation can be absolutely altered by disrupting the fruitless gene, so the precedence is there.
This recent study, which is quite timely after a hand bagging incident at work because of someone having an affair, shed some light the genetics of human pair bonding. It has been known for some time that the brain “hormone” arginine vasopressin (AVP) has an association with pair bonding in Voles. There are 3 species of closely related voles; montane voles (Microtus montanus), meadow voles (Microtus pennsylvanicus), and prairie voles (Microtus ochrogaster). The first 2 are non monogamous, whereas the prairie voles are monogamous. It was found that one of the proteins that recognizes the AVP; the vasopressin 1a receptor (V1aR) was responsible for the difference. Not surprisingly, drugs that affect the activity of this gene inhibited pair bonding in prairie voles. Furthermore, it was found that it was the promoter (control region) of the gene that determined the type of social bonding behaviour that developed, and a rather elegant study that swapped the promoter between species found that non monogamous voles could be made more like the monogamous species. The difference in promoters is an extra 428 base pairs. It is thought that this might alter the amount of V1aR in the relevant brain areas (ventral forebrain). Indeed, increasing the amount of V1aR in the ventral forebrains of non monogamous meadow voles turned them monogamous.
So, what about humans? Well, it turns out that the V1aR promoters comes in several different forms. One of these forms called the 334 allele has shown a strong correlation with marital harmony in studies of twins. There was no effect with women, but in partnerships where the man carried two copies of the 334 allele, 34% of marriages experienced a serious crisis/ threat of divorce in the last year. This figure fell to 15% in men with no copies of this allele. Interestingly, men with two copies were twice as likely to cohabit rather than marry when compared to men with no copies of the allele.
Other studies have also corroborated this by showing that 334 affects RNA (and by extension protein) levels in the hippocampus of post mortem subjects. Studies in healthy volunteers have also demonstrated an association between 334 and activation of the amygdala, a part of the brain already known to be involved in pair bonding.
It would be unlikely that only one gene affects this behaviour, and not surprisingly the dopamine system has also been implicated, so our pair bonding behaviour is probably the result of the interaction of several genes.
This recent study, which is quite timely after a hand bagging incident at work because of someone having an affair, shed some light the genetics of human pair bonding. It has been known for some time that the brain “hormone” arginine vasopressin (AVP) has an association with pair bonding in Voles. There are 3 species of closely related voles; montane voles (Microtus montanus), meadow voles (Microtus pennsylvanicus), and prairie voles (Microtus ochrogaster). The first 2 are non monogamous, whereas the prairie voles are monogamous. It was found that one of the proteins that recognizes the AVP; the vasopressin 1a receptor (V1aR) was responsible for the difference. Not surprisingly, drugs that affect the activity of this gene inhibited pair bonding in prairie voles. Furthermore, it was found that it was the promoter (control region) of the gene that determined the type of social bonding behaviour that developed, and a rather elegant study that swapped the promoter between species found that non monogamous voles could be made more like the monogamous species. The difference in promoters is an extra 428 base pairs. It is thought that this might alter the amount of V1aR in the relevant brain areas (ventral forebrain). Indeed, increasing the amount of V1aR in the ventral forebrains of non monogamous meadow voles turned them monogamous.
So, what about humans? Well, it turns out that the V1aR promoters comes in several different forms. One of these forms called the 334 allele has shown a strong correlation with marital harmony in studies of twins. There was no effect with women, but in partnerships where the man carried two copies of the 334 allele, 34% of marriages experienced a serious crisis/ threat of divorce in the last year. This figure fell to 15% in men with no copies of this allele. Interestingly, men with two copies were twice as likely to cohabit rather than marry when compared to men with no copies of the allele.
Other studies have also corroborated this by showing that 334 affects RNA (and by extension protein) levels in the hippocampus of post mortem subjects. Studies in healthy volunteers have also demonstrated an association between 334 and activation of the amygdala, a part of the brain already known to be involved in pair bonding.
It would be unlikely that only one gene affects this behaviour, and not surprisingly the dopamine system has also been implicated, so our pair bonding behaviour is probably the result of the interaction of several genes.
Anyone interested in the nature nurture debate may be interested in Matt Ridley’s talk here.
